Transcriptome-Wide Dynamics of m6A Methylation in Tumor Livers Induced by ALV-J Infection in Chickens

• Published in: Frontiers in immunology 2022-04, Vol.13, p.868892-868892
• Main Authors: Zhao, Qiqi, Yao, Ziqi, Chen, Liyi, He, Yaai, Xie, Zi, Zhang, Huanmin, Lin, Wencheng, Chen, Feng, Xie, Qingmei, Zhang, Xinheng
• Format: Article
• Language: English
• Subjects: ALV-J; co-expressed; Immunology; m6A; MeRIP-seq; RNA-seq
• ISSN: 1664-3224; 1664-3224
• DOI: 10.3389/fimmu.2022.868892

Avian Leukosis Virus Subgroup J (ALV-J) is a tumorigenic virus with high morbidity and rapid transmission. N6-methyladenosine (m 6 A) is a common epigenetic modification that may be closely related to the pathogenicity of ALV-J. Currently, there are no reports on whether m 6 A modification is related to ALV-J induced tumor formation. In this study, we used methylated RNA immunoprecipitation sequencing (MeRIP-seq) and RNA sequencing (RNA-seq) to examine the differences in m 6 A methylation and gene expression in normal livers and ALV-J-induced tumor livers systematically, with functional enrichment and co-expression analysis. The results identified 6,541 m 6 A methylated peaks, mainly enriched in CDS, and more than 83% of the transcripts contained 1-2 m 6 A peaks. For RNA-seq, 1,896 and 1,757 differentially expressed mRNAs and lncRNAs were identified, respectively. Gene enrichment analysis indicated that they may be involved in biological processes and pathways such as immunology-related and apoptosis. Moreover, we identified 17 lncRNAs, commonly existing in differently expressed methylome and transcriptome. Through co-expression analysis, 126 differentially expressed lncRNAs, and 18 potentially m 6 A-related methyltransferases were finally identified and connected, suggesting that m 6 A modifications might affect gene expression of lncRNAs and play a role in ALV-J induced tumor formation. This study provides the first comprehensive description of the m 6 A expression profile in tumor livers induced by ALV-J infection in chickens, which provides a basis for studying the role of m 6 A modification in ALV-J induced tumorigenesis. This study provides clues for studying the epigenetic etiology and pathogenesis of ALV-J.